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Microorganisms + Disease > Mechanisms of Pathogenesis L4 > Flashcards

Mechanisms of Pathogenesis L4 Flashcards

1
Q

what are the groups that pathogens are divided into

A

opportunistic pathogens

primary pathogens

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2
Q

what are opportunistic pathogens

A

Only cause serious disease when host defences are impaired

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3
Q

what are primary pathogens

A

Capable of causing disease in absence of immune defects

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4
Q

what do bacterial groups possess

A

virulence determinants which contribute to their ability to cause disease

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5
Q

if a pathogen has a single virulence is it pathogenic

A

Rarely is possession of a single virulence determinant sufficient to make a bacterium pathogenic
Virulence is Multifactorial relies on several things that the bacteria makes

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6
Q

what is the bacterial surface composition importance

A

mediates initial interactions with mammalian tissues and other surfaces
how the organism causes disease - bacterial virulence

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7
Q

what is the capsule

A

usually a polysaccharide layer, generally covers the whole bacterial surface

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8
Q

what is adhesion

A

fimbrae and pili are rod shape structures involved in sticking bacteria to surfaces

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9
Q

what are the envelope proteins for

A

some involved in adhesion, others involved in nutrient uptake, getting nutrient into the bacteria to grow

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10
Q

what contains lipopolysaccharide

A

only in gram negative bacteria

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11
Q

what is the function of lipopolysaccharide

A

Is important in immune invasion particularly complement invasion
Acts as a toxin, can induce damage

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12
Q

what happens between healthy to diseased

A

modulated by host immune responses

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13
Q

what happens when pathogen enters our tissues

A

immune system tries to remove
Bacteria can respond to get over the immune response
Dynamic equilibrium between the the bacteria and the immune system, depending which is ‘winning

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14
Q

what are the bacterial disease processes

A
  1. colonisation (adhesion, nutrient acquisition)
  2. tissue invasion
  3. avoidance of host defences
  4. tissue damage
  5. transmission
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15
Q

what is colonisation

A

First stage of disease process

Definition - Establishment of a stable population of bacteria in the host

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16
Q

where is bacteria available for colonisation

A

Source of bacteria is the environment, infected individuals or normal flora

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17
Q

what is the first interaction of bacteria in colonisation

A

Frequently on mucosal surface e.g respiratory tract (breathe organisms in), gastrointestinal tract (ingestion) or urogenital tract (sexual contact)

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18
Q

what is colonisation resistance caused by

A

Combination of host and bacterial factors which prevent colonisation by potential pathogens

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19
Q

examples of host factors that cause colonisation resistance

A
  • low gastric pH
  • bile
  • proteases
  • peristalsis
  • salivary and mucous flow
  • immunoglobulin A production
  • macrophages
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20
Q

bacterial factors that cause colonisation resistance

A

Include competition by normal flora for space, nutrients and receptors and production by bacteria of fatty acids and bacteriocins

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21
Q

why are lactobacilli important in colonisation

A

Lactobacilli in breast milk colonise gut in new born babies and prevent infection by E.coli
In the vagina, Lactobacilli metabolise glycogen, resulting in a low pH, limits colonisation by potential pathogens

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22
Q

what can occur if interfere with colonisation resistance

A

disruption of normal bacterial flora may result in removal of competition and overgrowth of normal flora
in low amounts they are ok, but overgrowth can cause disease

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23
Q

can antibiotics help with interference with colonisation resistance

A

Treatment with antibiotics may lead to overgrowth of Clostridium difficile and Staphylococcus aureus in the gut and Candida albicans in the mouth
act as opportunistic pathogens

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24
Q

what could allow colonisation of organisms not usually found in a particular site

A

impairment of normal physiological functions

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25
Q

how may bacterial overgrowth in mouth occur

A

Dehydration may reduce salivary flow

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26
Q

what must bacteria be able to do in mucosal surfaces

A

mucosal sites are physiologically flushed e.g saliva in the mouth, peristalsis in the gut
bacteria must adhere to cell surfaces
Some bacteria adhere to other surfaces

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27
Q

what are the adherence stages

A

attachment
adhesion
Subsequent stages may result in aggregation to produce a biofilm - associated with biomaterials e.g catheters

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28
Q

what may happen to biofilms in adherence

A

Biofilms may disperse and seed new sites of infection

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29
Q

what happens in the attachment stage

A

non-specific physicochemical properties of the bacterium and the target surface - charge and hydrophobicity
Bacterial and mammalian cell surfaces usually both have a nett negative charge, only allows bacterium to approach cell surface within approx 10nm

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30
Q

what is the attachment phase like

A

reversible and mediated by weak ionic interaction such as hydrogen bonding and Van der Waal’s forces

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31
Q

what occurs in adhesion stage

A

involves specific interactions between bacterial surface components (adhesins) and mammalian cell surface receptors
Interaction allows bacterium to become intimately associated with cell surface - overcoming repulsive forces associated with charge effects

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32
Q

what is adhesion like

A

usually considered to be an irreversible process

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33
Q

what is the biofilm made up of

A

composed of bacteria and associated molecules form a matrix in which the bacteria are embedded
made up of bacterial cells and an extracellular matrix made of proteins, polysaccharide and DNA

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34
Q

what are bioflims

A

Once attached, some bacteria continue to grow in association with the surface to form a multi-layered biofilm

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35
Q

can biofilms be removed by antibiotics

A

antibiotics may not penetrate or work on all cells in the biofilm

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36
Q

how do biofilms cause infection throughout the body

A

Biofilms may also disperse – and cause infection at other body sites

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37
Q

how do phagocytic cells ingest bacteria in the biofilm

A

Phagocytic cells cannot easily ingest bacteria in a biofilm

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38
Q

what are conditioning films

A

biomaterials are implanted into tissue, they very quickly become coated with host proteins e.g fibrinogen, fibronectin
coating of host proteins is referred to as a conditioning film

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39
Q

what do the conditioning films do

A

bacteria can adhere to “bare” biomaterials in vitro, in tissues the conditioning film components probably act as the major receptors to which bacteria adhere

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40
Q

adhesin examples

A

Fimbriae - rod like protein adhesins e.g E. coli

Polysaccharide adhesins e.g oral streptococci

41
Q

receptor examples

A

Blood group antigens

Extracellular matrix proteins (stick cells altogether) e.g fibronectin, collagen

42
Q

what is essential for bacterial growth

A

iron

43
Q

how much iron is available in our body for bacteria

A

Levels of free iron ion our tissues are very low (low as can be toxic to us)
not enough iron for need of bacteria

44
Q

how do bacteria get enough iron for growth

A

bacteria express high affinity iron uptake systems
two main systems:
1. Siderophores
2. Direct binding of host iron transport proteins

45
Q

what happens in the siderophore system

A

Bacteria sense not much iron available, switches on set of genes produce a siderophore, has a very high affinity of molecules with Fe3+ (ferric)
Siderophore interact with host tissue, has a higher affinity for the ferric than it does for the host tissue
Siderophore releases host tissue back into circulation, it uptakes the ferric
Goes to specific bacterial receptor on the surface, siderophore binds to receptor, is internalised into cell, iron is reduced to Fe2+
Fe2+ has lower affinity for siderophore, so is released and the bacteria can use it
Siderophore reused

46
Q

what happens in the transferrin binding receptor mechanism

A

Bacterium makes a receptor on the surface that specifically recognises transferrin
Transferrin in circulation with the ferric attached binds to the bacterium receptor
Transferrin cant be taken into cell as too big, iron removed from surface and taken into cell and transferrin released

47
Q

how is the Transferrin binding receptor mechanism limited

A

Only binds human transferrin – limits this organism

48
Q

when are high affinity iron uptake systems in use

A

Only expressed under conditions of iron limitation e.g in mammalian tissues

49
Q

what controls the expression of mechanisms for iron uptake

A

Expression controlled genetically by an iron dependent gene regulator called Fur
Fur = ferric uptake regulator
(controls amount of iron taken up as too much iron is also toxic for bacteria

50
Q

what happens when there is a lot of iron in the body

A

Fur protein ferric uptake regulator binds to iron that available in cell forms a dimer – dimerisation
Binds to specific dna sequence
Bound to promoter blocks transcription of gene

51
Q

what happens when there is not a lot of iron in body

A

deficient
no binding occurs
so gene can be transcribed to obtain iron from tissues

52
Q

what is invasion

A

Some bacteria are able to penetrate into, through or between cells

53
Q

why may invasion occur

A

may aid in survival and their spread to other body sites

54
Q

where do bacteria invade

A

some bacteria can invade epithelial cells
others invade phagocytic cells
adhesion to specific receptors usually first stage in invasion

55
Q

what are adhesins called

A

invasins

56
Q

what do complements do

A

kills many Gram-negative bacteria

Complement and antibodies target bacteria for destruction, promoting phagocytosis and killing

57
Q

what do cytokines do

A

allow cells to communicate with each other, can generate both antibody and phagocytic responses

58
Q

how do gram negative bacteria avoid complement

A

cause sepsis are complement resistant
Resistance due to lipopolysaccharide (LPS) on the bacterial surface
Polysaccharide side chains of LPS sterically hinder access of activated complement components to the bacterial membrane

59
Q

how can bacteria be complement resistant

A

Side chains prevent the membrane attack complex in the membrane

60
Q

what happens if bacteria is not complement resistant

A

membrane attack complex
insert through bacterial membrane and forms a pore, internal contents of bacteria seep, loss of bacterial contents will kill the bacteria

61
Q

can capsules aid avoidance of complements

A

prevent complement deposition or activation at an appropriate site e.g E.coli
Some bacteria also produce proteins which interfere with complement function - chemoattractant
protect against direct contact with complement

62
Q

avoidance of antibodies using a bacterial capsule

A

prevent antibody binding or are weakly antigenic, so prevent efficient phagocytosis (so not recognised doesn’t initiate response to clear them)
Many different capsular types may be produced

63
Q

avoidance of antibodies using antigenic variation

A

used by some bacteria to avoid binding of antibodies
Genetic mechanism allows it to change
New variant of protein is not recognised – avoid recognition
Why can be repeatedly infect

64
Q

avoidance of antibodies using antigenic mimicry

A

Some bacterial capsules are identical to mammalian tissue molecules so are not recognised as foreign
Structure similar to structures in our tissues
Not to recognise self
If can coat in host tissue wont recognise

65
Q

avoidance of antibodies using enzymatic digestion of antibodies

A

e.g Neisseria meningitidis produces an IgA protease
degrades IgA antibody on mucosal surfaces and prevents it from agglutinating bacteria
Produce enzymes – proteases that chop IgA, so antibody not functioning
prevents the agglutination of antibodies also

66
Q

how do bacteria avoid phagocytes

A

Some bacteria produce toxins which kill phagocytes or inhibit their migration to sites of infection
Inherent physical properties of some bacterial capsules inhibit phagocytosis

67
Q

how is the interaction of bacteria and phagocytes reduced further

A

hydrophilic capsule - phagocytic capsule like hydrophobic

68
Q

affect of alpha toxins

A

High conc of alpha toxins kills

Low conc of alpha toxins inhibits their migration

69
Q

how can some bacteria modify their response to cytokines

A

Some bacteria can modify normal cytokine responses and alter the immune response in favour of bacterial survival
Can interfere with direction immune response is directed – interfere with the cytokine response

70
Q

how can tissue damage occur

A
  1. Direct effects of bacterial toxins
  2. Indirect effects of bacterial toxins
  3. Induction of autoimmune responses(own cells attack by own immune system) bacterium contains proteins and antigens, some are nearly identical to some in our body
71
Q

what are the two types of bacterial toxins

A 
exotoxins
endotoxins (LPS)
72
Q

what do exotoxins do

A

actions selective for specific biochemical targets

73
Q

what do endotoxins do

A

activates many biochemical pathways - effects mediated by triggering of cytokine release from mammalian cells

74
Q

what do cytokines do

A

released include TNF –α (stimulate further tissue damage)

High concentrations cause cell/tissue damage

75
Q

what are exotoxins made by

A

gram +ve and -ve

76
Q

what are endotoxins made by

A

gram -ve

77
Q

what is an exotoxin

A

protein

78
Q

what is an endotoxin

A

lipopolysaccharide

79
Q

how are exotoxins released

A

secreted by living bacteria

80
Q

how are endotoxins released

A

cell lysis

81
Q

what happens to exotoxins and endotoxins when heated

A

exotoxins usually heat labile - proteins will denature

endotoxins usually heat stable

82
Q

what toxoids (vaccines) are there for exotoxins and endotoxins

A

exotoxins - toxoids available

endotoxins - no toxoids

83
Q

how lethal are exotoxins and endotoxins

A

exotoxins - potentially

endotoxins - lethal (higher conc)

84
Q

how are bacterial exotoxins classified

A

molecular mode of action

85
Q

what do type 1 exotoxins do

A

Bind to mammalian surface proteins and trigger transmembrane signals

86
Q

what do type 2 exotoxins do

A

Pore or channel forming toxins

87
Q

what do type 3 exotoxins do

A

Bind to surface receptors and translocate active component into the cell

88
Q

where are exotoxins generally located

A

cytoplasm of bacterial cell

89
Q

where are endotoxins generally located

A

outer membrane (surface layer of gram -ve bacteria)

90
Q

what makes up lipopolysaccharide

A

lipid A
core oligosaccharide
o-polysaccharide

91
Q

how is a pore formed in the membrane

A

Receptor on mammalian cell surface
Pore forming toxin bind
Aggregates to form multimer that forms a pore in the membrane

92
Q

what is the lipid A function in LPS

A

anchors molecules into outer membrane – very hydrophobic

93
Q

what is the o polysaccharide function

A

stop complement getting to bacterial membrane, also stimulate an immune response (can sometimes be protective)

94
Q

what are some properties of LPS

A
  • pyrogenic (gives you a fever)
  • potentially lethal
  • activates complement cascade (tissue damage)
  • activates clotting cascade
  • induces TNF - alpha production
  • induces interelukin 1 production
95
Q

what is transmission

A

Spread from host to host maintains bacterial pathogens in the population – otherwise they would die out if the infected host dies

96
Q

what is horizontal transmission

A

via direct contact, air, food, water, insect vectors

97
Q

why are spores able to survive in a lot of environments

A

survive in soil and water etc don’t dry out

98
Q

what is vertical transmission

A

mother passing on infection to neonates in utero

Microorganisms + Disease (16 decks)

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